Abstract

Introduction

Advanced glycation end products (AGEs) are produced and can accumulate during chronic
inflammation, as might be present in patients with rheumatoid arthritis (RA). AGEs
are involved in the development of cardiovascular disease. The aim of this study is
to evaluate whether AGEs are increased in patients with long-standing RA and whether
AGE accumulation is related to disease activity, disease severity and measures of
(premature) atherosclerosis, such as endothelial activation, endothelial dysfunction
and intima media thickness (IMT).

Results

AGEs were increased in RA patients (median 2.4 arbitrary units (a.u.), range 1.6 to
4.2) compared to HC (2.2, 1.3 to 3.8). RA patients had a DAS-28 score of 2.9 (0.8
to 6.9) and a modified Sharp-v.d. Heijde score of 19 (0 to 103). sVCAM-1 and vWF levels
were higher in RA patients. SAE was significantly decreased in RA (3.9 ml/mmHg (1.4
to 12.2) vs. 6.1 in HC (1.7 to 12.9). IMT did not differ between the two groups. Combining
both groups' AGEs correlated with vWF, sVCAM-1 and IMT, and was inversely related
to SAE. In RA, AGEs had an inverse relation with SAE, but did not relate to disease
activity or radiological damage. In multivariate analysis for both groups, smoking,
glucose levels, vWF, SAE and male gender were significantly related to the formation
of AGEs.

Conclusions

AGEs were increased in RA patients with long-standing disease and without signs of
premature atherosclerosis. AGEs were related to endothelial activation and endothelial
dysfunction. This supports the hypothesis that in RA AGEs may be an early marker of
cardiovascular disease.